Premature Ventricular Contractions

Home , Cardiac arrest, Syncope (medicine)

Matthew B. Sellers MD, MS Cardiac Electrophysiology AnMed Health Arrhythmia Specialists [email protected] Disclosures

• Under Accreditation Council for Continuing Medical Education guidelines, disclosure must be made regarding financial relationships with commercial interests within the last 12 months

• Matthew B. Sellers MD, MS

• I have no relevant financial relationships or affiliations with commercial interests to disclose Outline

• Case • Prevalence • Mechanism • Associated conditions • Clinical presentation • Evaluation • Prognosis Case • 68yo WM with CAD s/p inferior MI c/b ischemic cardiomyopathy (EF 45%), RBBB, PVCs, NSVT presented with frequent PVCs and symptoms of fatigue and shortness of breath

• No syncope, presyncope

• Holter: 36,000 PVCs (30%), periods of bigeminy, trigeminy and NSVT

• Intolerant to beta-blockers ECG Prevalence

• Duration of monitoring

• 1% on 12 lead ECG • 80% on 24 hour holter monitor Mechanism

• Re-entry

• Enhanced normal or abnormal automaticity

• Triggered activity Associated Conditions

• Hypertension with LVH • Acute myocardial infarction • Heart failure • Hypertrophic cardiomyopathy • Congenital heart disease • Idiopathic ventricular tachycardia • Other: OSA, COPD, pHTN, stimulants, endocrinopathies Clinical Presentation

• Asymptomatic • Palpitations, lightheadedness • Anxiety

• Palpitations  anxiety  catecholamine surge  ectopy  axiety

• Reversible cardiomyopathy Evaluation

• History, exam • 12 lead ECG • Ambulatory monitoring • Transthoracic echocardiogram • Exercise treadmill stress test

• ? Electrolytes, OSA screening, UDS Electrocardiography

• QRS duration > 120 msec

• Bizarre morphology (not typical aberration)

• T wave in opposite direction of main QRS

• Fully compensatory pause RVOT PVCs Prognosis in “Normal Hearts”

• ARIC  single PVC on 2 minute ECG had 2 fold increase in mortality from CHD • ARIC  2 fold increase in sudden cardiac death • Meta-analysis 8 prospective studies (3,629 persons) PVC was associated with increased all cause mortality, cardiovascular mortality, SCD, or ischemic CHD (OR 1.72, 95% CI 1.28-2.31) • Meta-analysis 106,195 persons  1 PVC on 10 second ECG or >30 in 1 hour recording associated with overall cardiac mortality (RR 2.1, 95% CI 1.7-2.5) and SCD • Several cohort studies report no clinical significance Exercise

• Withdrawal of vagal tone • Sympathetic stimulation increased circulating catecholamines • Increased HR, AV conduction, contractility • Increased cardiac output and oxygen delivery

• Initiate abnormal automaticity, triggered activity, re- entry Cellular Mechanisms Specific Conditions

• Exercise

• Structural heart disease

• Myocardial infarction

• CHF

Catecholaminergic PVT

• Inherited disorder • Syncope, sudden death • Presents in children and teenagers • Structurally normal heart • Normal ECG • VT elicited by physical and emotional stress • Bidirectional ventricular tachycardia • Syncope or cardiac arrest before 40 • Beta-blockers, ICD Bidirectional VT Acute MI

• PVCs are seen in the majority of MIs

• <48 hours  do not appear to affect prognosis

• Conflicting data after 48 hours

• PVCs carry a worse prognosis CHF

• PVCs are very common in CHF

• >10 per hour, incidence of NSVT is 90%

• Prior MI  associated with an increased risk of death, especially with LV dysfunction

• NSVT does not add additional risk Treatment

• Reserved for symptoms or cardiomyopathy

• Beta blockers, CCB

• Antiarrhythmic therapy

• Catheter ablation

CAST

• PVCs are associated with an increased risk of sudden and nonsudden cardiac death after MI

• 6 days to 2 years post MI • EF of less than 55% • Patients were randomly assigned after establishment of arrhythmia suppression

Catheter Ablation

• ACC/AHA Guidelines

• Frequent, symptomatic, monomorphic PVCs • > 10,000 PVCs on 24 hour monitor

• Drug resistant, or patient preference

• Ventricular arrhythmia storm initiated by single PVC

Conclusion

• Repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract is an underappreciated cause of unexplained cardiomyopathy.

• Successful ablation of the focal source of ventricular ectopy results in normalization of left ventricular function Case Conclusion Case Conclusion Conclusions

• Most patients have PVCs

• Symptoms, frequency

• Structural heart disease

• PVC cardiomyopathy is typically reversible with catheter radiofrequency ablation Questions